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腺苷并不介导猫肺血管床中三磷酸腺苷的肺血管舒张反应。

Adenosine does not mediate the pulmonary vasodilator response of adenosine 5'-triphosphate in the feline pulmonary vascular bed.

作者信息

Neely C F, Kadowitz P J, Lippton H, Neiman M, Hyman A L

机构信息

Department of Anesthesia, Tulane University School of Medicine, New Orleans, Louisiana.

出版信息

J Pharmacol Exp Ther. 1989 Jul;250(1):170-6.

PMID:2501475
Abstract

Adenosine and ATP produce dose- and tone-dependent responses in the feline pulmonary vascular bed. That is, at baseline (low) pulmonary vascular tone adenosine and ATP produce vasoconstrictor responses and at elevated pulmonary vascular tone adenosine and ATP produce vasodilator responses. The mechanism mediating the vasodilator responses to adenosine and ATP was investigated in the intact-chest cat under conditions of controlled pulmonary blood flow and left atrial pressure. When lobar vascular resistance was raised with U46619, intralobar injections of adenosine and ATP caused dose-related decreases in lobar arterial pressure. The pulmonary vasodilator responses to ATP and adenosine were not altered by atropine, propranolol, meclofenamate or cimetidine indicating that these responses were not mediated by the release of vasodilator prostaglandins or to activation of beta adrenergic, muscarinic or histamine (H2) receptors. The decreases in lobar arterial pressure in response to adenosine were reduced significantly by BWA1433U, an adenosine (P1) receptor antagonist. BWA1433U induced a parallel shift of the adenosine dose-response curve to the right; however, it had no significant inhibitory effect on the decrease in lobar arterial pressure in response to ATP. The P1 receptor antagonist in doses of 10 and 30 mg/kg i.v. had no significant effect on the vasodilator response to nitroglycerin. The present data suggest that vasodilator responses to adenosine in the feline pulmonary vascular bed are mediated by adenosine (P1) receptors, whereas responses to ATP are mediated by a different mechanism that does not involve release of a vasodilator prostaglandin.

摘要

腺苷和三磷酸腺苷(ATP)在猫肺血管床中产生剂量和张力依赖性反应。也就是说,在基线(低)肺血管张力时,腺苷和ATP产生血管收缩反应,而在肺血管张力升高时,腺苷和ATP产生血管舒张反应。在控制肺血流量和左心房压力的条件下,对完整胸腔猫体内介导对腺苷和ATP血管舒张反应的机制进行了研究。当用U46619提高叶血管阻力时,叶内注射腺苷和ATP会导致叶动脉压出现剂量相关的下降。对ATP和腺苷的肺血管舒张反应不受阿托品、普萘洛尔、甲氯芬那酸或西咪替丁的影响,这表明这些反应不是由血管舒张性前列腺素的释放介导的,也不是由β肾上腺素能、毒蕈碱或组胺(H2)受体的激活介导的。腺苷(P1)受体拮抗剂BWA1433U可显著降低对腺苷反应时叶动脉压的下降。BWA1433U使腺苷剂量反应曲线平行右移;然而,它对ATP引起的叶动脉压下降没有显著抑制作用。静脉注射剂量为10和30mg/kg的P1受体拮抗剂对硝酸甘油的血管舒张反应没有显著影响。目前的数据表明,猫肺血管床中对腺苷的血管舒张反应是由腺苷(P1)受体介导的,而对ATP的反应是由一种不同的机制介导的,该机制不涉及血管舒张性前列腺素的释放。

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